L5- Pulmonary Pathology III Flashcards by Connor Patrick

what are the 2 ways to classify Asthma

based on prior sensitization to allergen: atopic, non-atopic
based on triggers: drugs, occupational, environmental, seasonal, exercise

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Atopic Asthma:

(1) mechanism
(2) triggers
(3) age of onset
(4) FHx
(5) skin tests
(6) PMHx

1- type I hypersensitivity, IgE
2- environmental: dust, pollen, dander, food
3- childhood
4- yes, FHx present
5- immeadiate wheal and flare
6- allergic rhinitis, eczema

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Non-atopic Asthma:

(1) mechanism
(2) triggers
(3) age of onset
(4) FHx
(5) skin tests
(6) PMHx

1- bronchial hyper-irritability
2- viral respiratory infections, SO2, NO2, etc
3- less common, begins anytime
4- less common to have FHx
5- no skin test results
6- less common to have certain PMHx components

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Atopic asthma is a (1) type of reaction or body response. The (2) will be inhaled and elicit a response from (3) cells in (4) type people. (3) will release the following, (5), in order to cause (6).

1- type I hypersensitivity (IgE mediated)
2- allergen
3- TH2 cells
4- genetically predisposed individuals
5- IL-4, IL-5, IL-13
6- IgE mediated mast cell degranulation

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list the 3 most important CKs in Atopic Asthma pathogenesis, include their functions

(type I hypersensitivity reaction, IgE mediated, all released from TH2 cells)

IL-4: stimulates IgE production
IL-5: activates eosinophils
IL-13: stimulates mucus production + promotes IgE production from B-cells

All are used in order to promote IgE coating of mast cells => degranulation

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atopic asthma pathogenesis is split into (1) which presents at (2) time, and then (3) presenting at (4) time; this phenomenon is due to (5)

1/2- early phase, minutes
3/4- late phase, 4-24 hrs
5- two separate waves of mediators

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describe the components of the early phase of Atopic Asthma pathogenesis

(1st wave of mast cell degranulation, initiates in minutes)

bronchoconstriction (direct vagal nerve stimulation)
inc mucus production
vasodilation => inc permeability
further leukocyte recruitment

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describe the components of the late phase of Atopic Asthma pathogenesis

(2nd wave of mast cell degranulation, initiates 4-24 hrs later)

activation of eosinophils, PMNs, T-cells
epithelial activation –> TH2 cell and eosinophil recruitment

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Non-atopic asthma is usually caused by (1) and or (2). (1) will induce (3) which in turn will (4) in response to (2). (5) and (6) are critical similarities to atopic asthma.

1- secondary to viral infections
2- inhaled irritants: SO2, NO2, O3
3- virus induced mucosal damage
4- lower threshold of sub epithelial vagal receptors
5- inflammatory mediators
6- Tx

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(1) is the most common drug observed in drug-induced asthma. This results from (1) inhibiting (2) production and therefore increasing (3) production which are responsible for the asthma reaction, specifically (4). This will present as (5) clinically.

1- aspirin
2- TXs, PGs (dec)
3- LTs (inc)
4- LT mediated bronchoconstriction
5- recurrent rhinitis, nasal polyps, urticaria, bronchospasm

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list common triggers found in Occupational Asthma

fumes, organic dusts, chemical dusts, gases: epoxy resins / plastics, wood, cotton, platinum, toluene

*note- asthma attacks follow repeated exposure

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list the 2 main features of the gross appearance of asthma

occlusion of airways by thick mucus

- lung hyperinflation (due to obstruction)

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Asthma Histology:

(1) fluid changes
(2) epithelial changes
(3) observed in bronchial lumen
inc in total (4) cells
inflammation => inc (5) cells
(6) changes to bronchial smooth muscle cells
(7) changes to basement membrane

1- edema
2- patchy necrosis
3- mucus plugs with Curschmann spirals, Charcot Leyden crystals, eosinophils
4- goblet cells
5- eosinophils
6- SM hypertrophy and hyperplasia
7- thickened BM // sub-basement membrane fibrosis

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define:

(1) Curschmann spirals

(2) Charcot Leyden crystals

1- whorls of shed epithelium (necrotic cells)

2- collections of crystalloids formed by Protein Galactin-10 via eosinophils

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Asthma is defined as (1- include Sxs + its frequency) clinically. (2) is progressively trapped in lung because of (3). Attacks are considered (4) and last for (5).

1- recurrent sudden attacks of dyspnea, chest tightness, expiratory wheezing/ronchi, cough with thick sputum
2- air –> progressive hyperinflation
3- (air trapped distal to) mucus plug in bronchi
4- episodic (nights, early mornings)
5- hrs, subsiding spontaneously or with therapy

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define status asthmaticus

severe, prolonged asthma attack
non-responsive to therapy
NEEDS emergency management

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Physical Exam for Asthma:

(1) RR change
(2) on auscultation
(3) spirometry changes

1- tachypnea
2- expiratory (mostly) wheeze –> indicates obstruction
3- FEV1 <30%, inc all lung volumes, dec FEV1:FVC

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Laboratory Analysis for Asthma:

(1) seen in serum
(2) seen on ABG
(3) seen in sputum

1- eosinophilia
2- hypoxia, hypercapnia, respiratory acidosis
3- Curschmann spirals, Chracot Leyden crystals, eosinophils

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Eosinophilic Granuloma, aka (1), is a disease most found in (2) people. Patients usually present with (3) symptoms because of (4) changes in the lung. (5) are the ‘culprit cells’ and have (6) characteristic on histology.

1- pulmonary histiocytosis X / pulmonary Langerhan cell histiocytosis (PLCH)
2- smokers (cessation is apart of Tx)
3- dyspnea, cough
4- interstial nodular and fibrotic disease –> obstructive and restrictive changes on spirometry
5- Langerhans cells (not eosinophils)
6- Birbeck granules on EM

define the 3 components of bronchiectasis

*permanent dilation of bronchi/bronchioles
-> destruction of supporting tissue
-> due to or associated with chronic necrotizing infection

what are the 3 possible etiologies/causes of bronchiectasis

obstruction (tumor, foreign body) leading to localized bronchiectasis
congenital / hereditary conditions (CF, immunodeficiency, Kartagener’s)
Necrotizing/Suppurative pneumonia (virulent species: S. aureus, Klebsiella spp.)

list the few steps of Bronchiectasis Pathogenesis

1) Obstruction hampers clearance => pooling
2) secondary infection
3) damaged / weakened bronchial walls
4) bronchiectasis

describe the gross appearance of bronchiectasis

-marked dilated bronchi, filled with purulent mucus

dilation can be followed to pleural surfaces
dilated bronchi appear as cysts filled with mucopurulent secretions

Microscopic appearance of Bronchiectasis:

(1) initial bronchial wall changes
(2) later bronchial wall changes
(3) bronchial epithelial changes
(4) are possibly present, and (5) are usually positive in bronchiectasis

1- intense acute/chronic inflammatory exudate + necrotizing ulceration
2- fibrosis on bronchial walls –> bronchiolitis obliterans
3- squamous metaplasia
4- abscesses
5- cultures are usually positive

list the presenting symptoms of bronchiectasis

-*severe persistent productive cough with foul smelling sputum (infection is common determinant factor / trigger) - dyspnea, hemoptysis - clubbing, cyanosis

list the complications stemming from bronchiectasisi

- brain abscess (seeding microbe from lungs) - cor pulmonale - pulmonary HTN - amyloidosis

Kartagener Syndrome is apart of the (1) group of disorders. It is inherited in (2) fashion and is a disorder in (3) which impairs (4).

1- primary ciliary dyskinesia 2- AR 3- ciliary microtubules 4- impairs mucociliary escalator (clearance of lung secretions)

Kartagener Syndrome, a (1) type disorder, results in persistent (2) leading to (3). There is also decreased (4) in males leading to (5).

1- primary ciliary dyskinesia 2/3- lung infections --> bronchiectasis 4/5- dec spermatazoa motility --> sterility

list the main symptoms of components of Kartagener Syndrome

- bronchiectasis - chronic sinusitis - (1/3 of people) situs inversus

Restrictive Lung Disease involves the (1) of CT and the hallmark feature is (2).

1- inflammation and fibrosis of pulmonary CT | 2- involvement of interstitium

define the 3 synonyms for interstitial lung disease

Infiltrative: cellular and non-cellular infiltrates w/in alveolar septa/alveoli Restrictive: reduced TLC + normal/reduced expiratory flow rate DPLD (diffuse parenchymal): involves intra-alveolar space

list the components of lung interstitium

-basement membrane of endothelium and epithelium - collagen, elastin - fibroblasts, scattered mononuclear inflammatory cells (alveolar macrophages)

the etiopathogenesis for restrictive lung diseases is....

largely unknown

define alveolitis

damage to pneumocytes and endothelial cells (via inflammation)

Most restrictive lung disease involves (1) infiltration in the (2) part of the lung where (3) mediate and stimulate (4). (4) will lead to decreased (5) and increase (6) of the lung.

``` 1- leukocyte 2- interstitium 3- CKs 4- interstitial fibrosis 5- dec lung compliance (expansion) 6- inc elasticity (recoil) ``` 5/6 => dec lung expansion upon inspiration

The main feature of restrictive lung disease is (1) which leads to decreased (2) of the lung which presents as (3) symptom. (1) and damage to interstitium leads to (4) and presents as (5) symptoms.

``` 1- fibrosis 2- lung compliance / stiff lung (--> inc work to breath) 3- dyspnea 4- VQ mismatch --> hypoxia 5- tachypnea, cyanosis ```

describe spirometry results of Restrictive Lung Disease

- dec in all lung volumes - dec in flow rates - normal to inc FEV1:FVC - dec DLCO (diffusing capacities)

describe CXR results in Restrictive Lung Disease

bilateral infiltration: - nodular/reticular - ground-glass shadows / infiltrative

The main complications of restrictive lung disease is progression to....

- cor pulmonale | - pulmonary HTN

IPF = (1) / (2): - (3) etiology - males (=/>) females - (5) age group - (6) prognosis

``` 1- idiopathic pulmonary fibrosis 2- UIP, usual interstitial pneumonia 3- unknown 4- M > F 5- 2/3 > 60 y/o (mean is 40-70 yrs) 6- poor (5 yr survival is 20%, mean survival is <3 yrs) ```

IPF/UIP has progresses to (1) leading to (2). Its progression is described as (3). (4) is the main treatment protocol.

``` (idiopathic pulmonary fibrosis, usual interstitial pneumonia) 1- bilateral fibrosis 2- severe hypoxia, cyanosis 3- relentless (=> poor prognosis) 4- lung transplantation ```

IPF and UIP will have insidious onset of (1) and (2). (3) will be present on auscultation. In the late stages, the following will become more apparent: (4).

``` (idiopathic pulmonary fibrosis, usual interstitial pneumonia) 1- dry cough 2- exertional dyspnea 3- crackles on inspiration 4- cyanosis, cor pulmonale, clubbing ```

describe the radiographic appearance of IPF/UIP (indicate which processes / diseases must be ruled out)

(idiopathic pulmonary fibrosis, usual interstitial pneumonia) - restrictive pattern: inc interstitial markings (fibrosis) + Honey Comb appearance - fibrosis is mainly in lower lobes bilaterally

describe the gross appearance of the lung in IPF/UIP

(idiopathic pulmonary fibrosis, usual interstitial pneumonia) - cobble-stoned pleural surface - honeycomb cysts -firm, fibrotic parenchyma with lower lobe and subpleural accentuation

IPF/UIP Histology: - (1) hallmark feature - (2) is the difference of (1) in different places, therefore (3) and (4) by co-exist - worse in (5) areas

(idiopathic pulmonary fibrosis, usual interstitial pneumonia) 1- patchy interstitial fibrosis 2- temporal (time) and geographic (spatial) heterogeneity 3- mature fibrosis 4- young fibroblast foci 5- accentuation beneath pleura and along interlobular septa Note- some areas are spared, normal lung

describe the honeycomb changes in IPF/UIP

(idiopathic pulmonary fibrosis, usual interstitial pneumonia) - cystic spaces lined by type II pneumocytes / respiratory epithelium - dense fibrosis destroys architecture of parenchyma --> cysts